Livin, Survivin and Caspase 3 as early recurrence markers in non-muscle-invasive bladder cancer

Wang, Jianwen; Zhang, Xiaodong; Wei, Ping; Zhang, Junhui; Niu, Yinong; Kang, Ning; Zhang, Yuxiang; Zhang, Weili; Xing, Nianzeng

doi:10.1007/s00345-014-1246-0

Cited by 27 publications

(22 citation statements)

References 24 publications

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“…Expression of tumor suppressor proteins that restrict cell cycle progression and cell survival is inhibited in bladder cancers (23). In addition, reduced expression of apoptotic proteins, such as Fas and Caspase-3 is linked to poor outcome in patients with bladder cancer (24,25). In our results we demonstrate that hyperforin significantly induces apoptosis and extrinsic/intrinsic apoptotic signaling (increases of active-Fas, FasL, Caspase-8 and loss of mitochondrial membrane potential) in TSGH-8301.…”

Section: Discussionsupporting

confidence: 50%

Hyperforin Induces Apoptosis Through Extrinsic/Intrinsic Pathways and Inhibits NF-ĸB-modulated Survival and Invasion Potential in Bladder Cancer

Liu

Lin

Hsieh

et al. 2019

In Vivo

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Background/Aim: Muscle-invasive bladder cancer (MIBC) has long been recognized as a difficult to treat cancer type, thus a new treatment strategy is needed. The major purpose of the present study was to verify the anticancer effect of hyperforin and the mechanism through which it affects tumor cell growth and invasion in bladder cancer in vitro. Materials and Methods: Bladder cancer TSGH-8301 cells were treated with different concentrations of hyperforin for different durations of time. The changes in cell viability, production of calcium and reactive oxygen species (ROS), and anti-apoptotic signaling were evaluated using MTT assay, flow cytometry, and western blot analysis. The effect of hyperforin on the expression of nuclear factor-kappaB (NF-ĸB) p65 (Ser276), tumor progression-associated proteins, as well as on cell invasion was investigated using western blotting and cell invasion assay, respectively. Results: Hyperforin significantly induces apoptosis, extrinsic/intrinsic apoptotic signaling,

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Section: Discussionsupporting

confidence: 50%

Hyperforin Induces Apoptosis Through Extrinsic/Intrinsic Pathways and Inhibits NF-ĸB-modulated Survival and Invasion Potential in Bladder Cancer

Liu

Lin

Hsieh

et al. 2019

In Vivo

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“…As far as we known, the caspases, Bcl-2, Bcl-xL and PARP were related to cell apoptosis in bladder cancer [20, 21]. Thus, we measured the activation of Bcl-2/caspases pathway.…”

Section: Resultsmentioning

confidence: 99%

HnRNP-L mediates bladder cancer progression by inhibiting apoptotic signaling and enhancing MAPK signaling pathways

Xing

et al. 2017

Oncotarget

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Heterogeneous nuclear ribonucleoprotein L (hnRNP-L) is a promoter of various kinds of cancers, but its actions in bladder cancer (BC) are unclear. In this study, we investigated the function and the underlying mechanism of hnRNP-L in bladder carcinogenesis. Our results demonstrated that enhanced hnRNP-L expression in BC tissues was associated with poor overall survival of BC patients. Depletion of hnRNP-L significantly suppressed cell proliferation in vitro and inhibited xenograft tumor growth in vivo. Furthermore, downregulation of hnRNP-L resulted in G1-phase cell cycle arrest and enhanced apoptosis accompanied by inhibition of EMT and cell migration. All these cellular changes were reversed by ectopic expression of hnRNP-L. Deletion of hnRNP-L resulted in decreased expression of Bcl-2, enhanced expression of caspases-3, -6 and -9 and inhibition of the MAPK signaling pathway. These findings demonstrate that hnRNP-L contributes to poor prognosis and tumor progression of BC by inhibiting the intrinsic apoptotic signaling and enhancing MAPK signaling pathways.

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“…Caspase‐3‐modulated deoxyribonucleic acid (DNA) fragmentation and cleavage of poly (ADP‐ribose) polymerase 1 (PARP1) can be activated by extrinsic and intrinsic apoptotic pathways . Decreased expression of Fas and Caspase‐3 is associated with poor prognosis in patients with bladder cancer . PARP1, an ADP‐ribosylating enzyme, participates in repair of various forms DNA damage and maintains chromatin remodeling .…”

Section: Discussionmentioning

confidence: 99%

“…23 Decreased expression of Fas and Caspase-3 is associated with poor prognosis in patients with bladder cancer. 21,24 PARP1, an ADP-ribosylating enzyme, participates in repair of various forms DNA damage and maintains chromatin remodeling. 25 Overexpression of PARP1 has been found in high stage cancers.…”

Section: Discussionmentioning

confidence: 99%

Regorefenib induces extrinsic/intrinsic apoptosis and inhibits MAPK/NF‐κB‐modulated tumor progression in bladder cancer in vitro and in vivo

Chiang

Chung

Hsu

2019

Environmental Toxicology

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The aim of the present study is to investigate anticancer effect and mechanism of regorafenib in bladder cancer in vitro and in vivo . Human bladder cancer TSGH 8301 cells were treated with regorafenib, NF‐κB, AKT, or mitogen‐activated protein kinase (MAPK) inhibitors for different time. The changes of cell viability, NF‐κB activation, apoptotic signaling transduction, and expression of tumor progression‐associated proteins were evaluated with MTT, NF‐κB reporter gene assay, flow cytometry, and Western blotting assay. TSGH 8301 tumor bearing mice were established and treated with vehicle (140 μL of 0.1% DMSO) or regorafenib (10 mg/kg/day by gavage) for 15 days. The changes of tumor volume, body weight, NF‐κB activation, MAPK activation, and tumor progression‐associated proteins (MMP‐9, XIAP, VEGF, and Cyclin‐D1) after regorafenib treatment were evaluated with digital caliper, digital weight, and ex vivo Western blotting assay. Our results demonstrated NF‐κB activation and protein levels of MMP‐9, XIAP, VEGF, and Cyclin‐D1 were significantly reduced by NF‐κB (QNZ), ERK (PD98059), and P38 (SB203580) inhibitors. Regorafenib also significantly induced extrinsic and intrinsic apoptotic signaling transduction in bladder cancer in vitro . In addition, regorafenib significantly inhibited tumor growth, NF‐κB, p38, ERK activation and expression of tumor progression‐associated proteins in bladder cancer in vitro and in vivo . Taken together, these results proved that regorafenib not only induced apoptosis through extrinsic and intrinsic pathways and but suppressed MAPK/ NF‐κB‐modulated tumor progression in bladder cancer.

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Livin, Survivin and Caspase 3 as early recurrence markers in non-muscle-invasive bladder cancer

Abstract: Livin, Survivin and Caspase 3 may be valuable as promising indicators of early recurrence in NMIBC.

Cited by 27 publications

References 24 publications

Hyperforin Induces Apoptosis Through Extrinsic/Intrinsic Pathways and Inhibits NF-ĸB-modulated Survival and Invasion Potential in Bladder Cancer

Hyperforin Induces Apoptosis Through Extrinsic/Intrinsic Pathways and Inhibits NF-ĸB-modulated Survival and Invasion Potential in Bladder Cancer

HnRNP-L mediates bladder cancer progression by inhibiting apoptotic signaling and enhancing MAPK signaling pathways

Regorefenib induces extrinsic/intrinsic apoptosis and inhibits MAPK/NF‐κB‐modulated tumor progression in bladder cancer in vitro and in vivo

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